In this issue of Blood, Tracy et al~1 describe a key subset of exhausted CD4~~+ T cells in Philadelphia chromosome positive (Ph~+) B-cell acute lymphoblastic leukemia (B-ALL) that modulates antileukemic effects. The authors use a nonirradiated immunocompetent murine model of Ph~+ B-ALL and primary patient samples to dissect the CD4 T-cell immune response and to provide a rationale for combination therapies of tyrosine kinase inhibitors that target the BCR-ABL oncoprotein and programmed death-ligandl (PD-L1) blockade to reverse the exhausted state of CD4~+ T cells and enhance the clearance of leukemia.
NSTL
Amer Soc Hematology
